Viral-induced lymphoreticular neoplasms were first characterized in mice and rats, and later in chickens and turkeys. In 1964, viruses were also found to be associated with lymphoid malignancies of cats. The virus was named the Feline Leukemia Virus (FeLV). FeLV is classified as an oncornavirus (onco=oncogenic or cancer producing and RNA=ribonucleic acid). This virus is very unstable in the environment and seldom survives for more than several hours at room temperature. It is inactivated by most disinfectants. FeLV occurs in three antigenically similar types, A, B, and C, or combinations of these types.
Infection results by contact between infected and susceptible cats. Infected cats may appear totally asymptomatic or they man manifest feline leukemia disease. The incidence of infected cats in the general population is somewhat variable, but has been reported to be as low as a few of tenths of a percent to in excess of several percent depending upon locality. The incidence of infected cats in catteries well known FeLV-related diseases is much higher and has been reported to average 30% or more. The overall mortality to FeLV is proportional to the percentage of cats that become persistently viremic following exposure and infection. It is not surprising, therefore, that catteries and multiple-cat households have a greater loss than the general cat population because the carrier rate in these environments is much greater. In the general urban cat population, it has been estimated that the total death rate to FeLV could possibly be as high as 350 per 100,000. In catteries where FeLV is endemic, the death rate is potentially as high as 1 in 3 or more.
The pathogenesis of FeLV infection can be divided into three stages: primary disease, recovery or apparent recovery, and terminal illness. By and large, only those cats or kittens which eventually become persistently viremic will show significant clinical signs of illness in the primary stage of infection. Clinical symptons consist of varying degrees of fever, malaise, anorexia, weight loss, generalized lymphadenopathy, and hematological abnormalities. Death can occur in the primary stage of infection and when it does it is usually a direct consequence of severe bone marrow suppression and/or secondary infection. Cats that recover completely from the infection usually do not show any clinical or hematological abnormalities in the primary stage of the disease. In contrast, kittens or cats that develop clinical and hematological abnormalities during the primary stage of disease usually become persistent virus carriers. It is interesting to note that relatively few kittens or cats die as a result of this primary illness. In fact, most persistently infected cats will apparently recover from these primary symptons, giving the veterinarian and the owner a false sense that recovery is complete and that the virus has been eliminated. Carrier cats may remain asympomatic for weeks, months, years, or even an entire natural lifetime. Many of these cats, however, will eventually develop some FeLV-related disease.
Persistent virus carrier cats can be expected to develop a fatal FeLV-related illness at the rate of about 20% per year for every year they remain infected. The mortality can be greater if symptomatic treatment is not given, or if the animals are stressed. This means that about 50% of chronic FeLV carriers will be dead within four years or less. In addition to a fatal disease, persistent virus carriers frequently suffer from vague persistent or intermittent illnesses and secondary infections of a number of types. Those diseases related directly to the effect of the virus include neoplastic disease, bone marrow suppressive disorders, immunological disorders, reproductive problems, and various miscellaneous diseases. Those diseases indirectly related to FeLV infection include viral and bacterial secondary infections, protozoal diseases, and other maladies. In terms of total disease caused by FeLV, vague illness and secondary infections are the most frequent. This is followed in order of frequency by bone marrow supressive disorders, lymphoproliferative neoplasms, and myeloproliferative disease.
Prior proposals aimed at producing a vaccine for preventing FeLV include that of Jarrett ("The Development of Vaccines Against Feline Leukemia", Origins of Human Cancer, pp 1215-1222, 1977) and Jarrett et al (U.S. Pat. Nos. 3,966,907, 4,034,081, and 4,086,134) wherein the vaccine is based on virus which are killed (e.g. by irradiation, hydroxylamine, or paraformaldehyde) or inactivated (e.g. by mitomycin D) or based on whole live infected cells and inactivated infected cells. Pinter et al in Viriology, 83, 417-422 (1977) and 91, 345-351 (1978) and in Journal of Viriology, 30, 157-165 (1979) report the formation of non-denatured [gp90] a naturally occuring disulfide complex of gp70 and pl5(E) virion antigens which may serve as the basis of a vaccine. None of these vaccines is truly effective in preventing disease caused by feline leukemia virus.